study on angiotensin converting enzyme gene insertion/deletion polymorphism and serum cortisol among a sample of egyptian patients with major depression disorder

ABSTRACT

Angiotensin-converting enzyme [ACE] is assumed to influence the activity of the hypothalamic-pituitary-adrenocortical [HPA] system, which shows hyperactivity in the majority of patients with major depression. The ACE gene, known to be associated with cardiovascular disorders, which in turn are accompanied with an increased susceptibility for depression, is therefore a promising candidate gene for effective disorders. However, the results are conflicting, with no reported studies on Egyptian depressed patients. This study aimed to assess ACE insertion / deletion [I/D] gene polymorphism among Egyptian depressed patients in order to clarify HPA system dysregulation, and to determine its possible association with severity of depression. This case/control study was conducted on 42 adult depressed patients, and 37 healthy controls were screened to detect genetic associations with unipolar major depression. Determination of ACE genotypes was performed for all subjects by real time PCR. Total serum cortisol levels were measured by ELISA. The frequencies of the DD, ID and II genotypes were 26.2%, 45.2%,and 28.2%, respectively among the cases, and 17.49%, 25.2%, and 56.41%3 respectively among the controls. Significant differences in ACE gefiotype distribution were observed between cases and controls [p - 0.0384]. Serum cortisol in patients show the highest value in the ID polymorphism while II polymorphism shows the lowest value of a.m. cortisol. Data illustrated a significant association of ID polymorphism with the more severity of illness. Our findings support that ACE gene I/D polymorphism and high D allele frequency are associated with depression, also hypercortisolimia is significantly higher in individuals with major depression compared to control among Egyptian adults. ACE gene polymorphism might provide a common link between developing depressive episode and dysfunctional HPA-axis